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Ayurveda Renaissance – Quo Vadis?
Published in D. Suresh Kumar, Ayurveda in the New Millennium, 2020
Several methylated sequences of vāta prakṛti were found to be represented in biological processes like cell communication, transcription, signal transduction pathways and embryo morphogenesis. The associated genes are involved especially in neuronal development. Additionally, the NFIX gene was found to be associated with low body mass index (B.M.I.) which is one of the characteristic signs of vāta prakṛti (Rotti et al. 2015).
Homeostasis of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Beyond neurotransmission, the SNARE proteins are involved in many biological functions during embryonic development, including fertilization, neural development, and synaptic plasticity. Homozygous deletion of the snap25 gene in mice results in embryonic lethality, while heterozygous deletion results in mice with small eyes due to failure to separate the cornea from lens epithelium during eye development. Such mice also exhibit head bobbing and locomotor hyperactivity [77]. Given their central role in neurotransmitter release, several genes related to the SNARE complex such as SNAP25, VAMP1, VAMP2, STX1A, SYT1 and SYT2 have been examined in psychiatric disorders. Although genome-wide association studies have not yet implicated the above genes in specific disorders, several SNARE polymorphisms have been associated with attention deficit hyperactivity disorder, autism spectrum disorders, major depressive disorder, bipolar disorder, and schizophrenia susceptibilities [77].
Neurological Activities of Seaweeds and their Extracts
Published in Leonel Pereira, Therapeutic and Nutritional Uses of Algae, 2018
Neurite outgrowth is a fundamental neuronal feature and plays an important role in neuronal development during embryogenesis and in the adult brain (Khodosevich and Monyer 2010). Sargassum macrocarpum and its two active components, sargaquinoic acid and sargachromechanol, have been shown to promote neurite outgrowth in pheochromocytoma (PC12) cells in rats (Kamei and Sagara 2002, Tsang and Kamei 2004, Tsang et al. 2005). Structure of sargaquinoic acid and neurite outgrowth promoting relationship has been reported by Tsang et al. (2001). They reported that quinone is the structural moiety of the sargaquinoic acid molecule, which is responsible for the neurite outgrowth-promoting activity. Notably, the hydroxyl group bonded to quinone had a significant effect on neuritogenic activity. In addition, pheophytin a, a chlorophyll-related compound and its analog, vitamin B12 derived from Sargassum fulvellum, also has potential neurite outgrowth-promoting activity (Ina and Kamei 2006, Ina et al. 2007).
Morphological study of the postnatal hippocampal development in the TRPV1 knockout mice
Published in Temperature, 2023
Melinda Boros, Noémi Sóki, Abigél Molnár, Hajnalka Ábrahám
While most of the hippocampal neurons reveal rapid pre- and postnatal neurochemical and morphological development and have adult-like morphology in the first postnatal week, certain interneuron types have long-lasting neurochemical development, such as the fast-spiking parvalbumin (PV)-containing axo-somatic and axo-axonic interneurons. These neurons start to express parvalbumin only at the end of the first postnatal week in the rodent hippocampal formation, and PV-immunoreactivity reaches an adult like pattern not before the third week of age [42,43]. Myelination is the last step of neuronal development and occurs after neurons were formed and established synaptic connections with their target cells. Myelination starts in the cerebral cortex including the corpus callosum at the postnatal day 3, when the first oligodendroglial cells are visible based on the presence of myelin-basic protein (MBP) that is expressed in the cells before the formation of myelin sheaths [44–47; 48]. In the hippocampus the first myelinated axons appear in the second half of first postnatal week and myelination lasts until the first months [49].
Could low α-N-acetylgalactosaminidase plasma concentration cause schizophrenia?
Published in The World Journal of Biological Psychiatry, 2023
According to the neurodevelopmental hypothesis, although the causes of schizophrenia are related to abnormal prenatal changes, the onset of the disease occurs at advanced ages, such as the second decade of life. There might be several approaches related to this issue. It is thought that until postnatal brain development is complete (this process continues into late adolescence or even early adulthood), brain regions without the disease compensate for the impaired brain regions. Another approach is the interaction of disease-causing factors with normal neuronal development (Hariri et al. 1999; Lieberman 1999). In our study, the mean age of onset of the disease was 20.56 ± 1.91. And there was a positive correlation between disease onset age and α-NAGAL levels. Those with earlier disease onset had lower enzyme concentrations. The possible explanation for this result may be that low α-NAGAL levels exacerbate the underlying pathology, leading to the onset of the disease at an earlier age.
Study on the ameliorating effect of miR-221-3p on the nerve cells injury induced by sevoflurane
Published in International Journal of Neuroscience, 2021
Qirui Wang, Xin Tian, Qijuan Lu, Kun Liu, Jiekun Gong
To observe the effects of sevoflurane on hippocampal neurons viability and apoptosis, the sevoflurane model was constructed, and cells were treated with the concentration of 1%, 2% and 3% sevoflurane, respectively. Neural development is a complex and dynamic process, and the viability of neural stem cells directly affects neural development. Drug-induced neuronal apoptosis is also a potential factor affecting neural development [24, 25]. Anesthetic drugs can trigger abnormal apoptotic patterns, and cause neurodegenerative changes in the brain [26]. It has shown that the exposure of sevoflurane may lead to the loss of hippocampal neurons and cognitive dysfunction by inducing the apoptosis of hippocampal cells mediated by endoplasmic reticulum stress [27]. This study revealed the toxic effects of sevoflurane on hippocampal neurons in rats, sevoflurane inhibited the cell viability and promoted apoptosis. These results were consistent with previous studies by Xu Yang et al [28]. Importantly, we observed that miR-221-3p level was decreased by sevoflurane, suggesting that the down-regulation of miR-221-3p was involved in the neuron injury induced by sevoflurane.